Third Quarter 2014 Financial Results and Corporate Update 1 Safe Harbour Forward Looking Statement This presentation contains forward-looking statements about ProMetic’s objectives, strategies and businesses that involve risks and uncertainties. These statements are “forward-looking” because they are based on our current expectations about the markets we operate in and on various estimates and assumptions. Actual events or results may differ materially from those anticipated in these forwardlooking statements if known or unknown risks affect our business, or if our estimates or assumptions turn out to be inaccurate. Such risks and assumptions include, but are not limited to, ProMetic’s ability to develop, manufacture, and successfully commercialize value-added pharmaceutical products, the availability of funds and resources to pursue R&D projects, the successful and timely completion of clinical studies, the ability of ProMetic to take advantage of business opportunities in the pharmaceutical industry, uncertainties related to the regulatory process and general changes in economic conditions. You will find a more detailed assessment of the risks that could cause actual events or results to materially differ from our current expectations in the Annual Information Form for the year ended December 31, 2013, under the heading “Risk Factors”. As a result, we cannot guarantee that any forward-looking statement will materialize. We assume no obligation to update any forward-looking statement even if new information becomes available, as a result of future events or for any other reason, unless required by applicable securities laws and regulations. All amounts are in Canadian dollars unless indicated otherwise. Copyright notice The information contained in this presentation (including names, images, logos and descriptions portraying ProMetic's products and/or services) is the property of ProMetic Life Sciences Inc., of its divisions and / or of its subsidiaries (“ProMetic”) and is protected by copyright, patent and trademark law and / or other intellectual property rights. Neither this presentation nor any part may be reproduced or transmitted in any form or by any means, electronic or mechanical, including printing and photocopying, or by any information storage or retrieval system without prior permission in writing from ProMetic. Disclaimer ProMetic reserves the right to make improvements, corrections and/or changes to this presentation at any time. 2 AGENDA Q3 2014 Milestones Guidance for H2 2014 Q3 financials Q3 Corporate Update: - Vanderbilt University Study - PBI-4547 poster - Clinical trial for 4050-DKD Milestones to year end – Outlook for 2015 3 Q3 2014 Highlights Fibrinogen commercial launch announced for Q4 2014 Development and scale-up of new affinity resin for multinational client $20 million follow-on investment from Thomvest Promotion of Mr. Pritchard to newly created position of COO Successful Pre-IND FDA meeting for PBI-4050 Inclusion of PLI to S&P/TSX Small Cap Index Clearance by FDA of plasminogen IND and clearance of pbi4050 CTA by Health Canada (Q4-14 events) 4 H2 2014 GUIDANCE • PBI-4050 to progress in patients – phase Ib • To disclose New PBI-4050 data at ASN (American Society of Nephrology Annual Meeting Nov 12-15) • To disclose an additional Orphan indication for PBI-4050 • To file the IGIV IND with the FDA • To disclose 2 additional PPPS™ derived Orphan Rx • To close partnering deals providing : • Financial contribution • Access to market • Additional manufacturing capacity • Revenue range for H2 2014 ($15 M - $20 M) • Subject to revenue recognition on licensing fees • Revenue significantly higher in Q4 5 Third Quarter 2014 Financial Results 6 Sources of Financial Information The following information is derived from: The financial information for the third quarters of 2014 and 2013, which have been reviewed by Ernst & Young, the Corporation’s Auditor; and the audited financial statements for 2013. All financial information has been prepared in accordance with International Financial Reporting Standards (IFRS). Further financial information, including the ProMetic’s Annual Information Form, is available on SEDAR (www.sedar.com). All tabulated sums are in CAD 000’s except for “per share” amounts or where indicated. 7 Year‐To‐Date Revenues: $M 16 14 12 8,8 5,1 10 8 6 4 6,8 7,3 YTD 2013 YTD 2014 2 0 Product Sales Service & Licensing Revenues 8 Third Quarter 2014: Results Quarter ended September 30 2014 2013 CAD 000s CAD 000s Revenues Cost of Goods Total Research & Development Costs Administration & Marketing Finance Costs Fair Value adjustment on Warrants Gain on revaluation of Equity Investment Purchase Gain on Business Combination Net Loss Net Loss per share (basic) EBITDA* YTD ended September 30 2014 2013 CAD 000s CAD 000s 2,315 5,960 12,464 15,566 867 7,846 3,006 774 10,420 ‐ ‐ 1,547 4,618 1,981 467 2,622 ‐ ‐ 4,659 23,397 7,883 1,825 12,432 (24,258) (8,065) 4,667 12,409 4,570 1,128 2,622 ‐ ‐ (20,677) (5,303) (5,919) (9,896) (0.04) (0.01) (0.01) (0.02) (7,668) (1,738) (19,688) (5,006) *EBITDA is a non‐GAAP measure, employed by the Corporation to monitor its performance. Therefore it is unlikely to be comparable to similar measures presented by other companies. The Corporation calculates its EBITDA by subtracting from Revenues, its Cost of Goods Sold, its Research and Development Expenses Rechargeable and Non‐Rechargeable as well as its Administration and Marketing Expenses and excluding depreciation of capital assets and licenses, amortization of licenses and patents and share‐based payments. 9 Comparison of Key Financials : Balance Sheet 30 September 2014 CAD 000s 10,383 31 December 2013 CAD 000s 17,396 4,928 14,172 12,893 9,631 104,743 4,663 Trade & Other Payables 6,098 7,877 Deferred Revenues 1,536 984 Warrant Liability 21,743 9,311 Long –term Debt (Thomvest) 22,291 6,217 ‐ 3,040 42,400 18,638 137,955 49,872 Selected information Cash Accounts Receivable Capital Assets Intangible Assets Long‐term Debt Provided by Shareholders Total Equity Balance Sheet Total Assets 10 10 Third Quarter 2014 Corporate Update 11 Vanderbilt University Study PBI‐4050 protects against the development of diabetic nephropathy (DN) in db/db eNOS‐/‐ mice Raymond C. Harris, Ming‐Zhi Zhang Vanderbilt University School of Medicine 12 Vanderbilt University Study db/db eNOS knockout Mouse model 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. Dramatic albuminuria GFR , SCr Hypertension (vs. db/db) Mesangial expansion Mesangiolysis Nodular glomerulosclerosis Arteriolar hyalinosis Macrophage infiltration Glomerular fibrin & hyaline deposition GBM thickening Tubulointerstitial injury Normal aorta, no atherogenic lesions Hyperinsulinemia, large islets Lower plasma glucose levels 13 Vanderbilt University Study Proteinuria is significantly increased in db/db mice with eNOS-/* * albumin/creatinine (g/mg) 1500 BKS eNOS-/db/db db/db/eNOS-/- 1250 1000 750 500 250 16 weeks of age 24 weeks of age 14 Vanderbilt University Study 15 Vanderbilt University Study 16 Vanderbilt University Study Late treatment with PBI-4050 protects against diabetic nephropathy in db/db eNOS-/- mice PBI-4050 Outer medulla Corte x Vehicle Masson’s trichrome staining: original magnification: 160 X Selectively colors collagen in blue 17 Vanderbilt University Study Late PBI-4050 treatment reduces kidney fibrosis (collagen 1) in db/db eNOS-/- mice Vehicle PBI-4050 Collagen I Collagen I staining. X400. 18 Vanderbilt University Study Late PBI-4050 treatment reduces kidney fibrosis (collagen IV) in db/db eNOS-/- mice Vehicle PBI4050 Collagen IV Collagen IV staining. X400. 19 Vanderbilt University Study Late PBI-4050 treatment reduces myofibroblasts in db/db eNOS-/- mice Vehicle PBI-4050 α-SMA, a marker of myofibroblasts. X160. 20 Vanderbilt University Study Late PBI-4050 treatment reduces kidney macrophage infiltration in db/db eNOS-/- mice Vehicle PBI-4050 Dark spots are Macrophages Infiltrating the kidney F4/80 staining, a marker of macrophages. 160 X 21 Vanderbilt University Study Late PBI-4050 treatment reduces kidney oxidative stress in db/db eNOS-/- mice Vehicle PBI-4050 Nitrotyrosine staining, a marker of oxidative stress. X100. 22 Vanderbilt University Study Late PBI-4050 treatment reduces kidney CTGF in db/db eNOS-/- mice Vehicle PBI4050 CTGF staining, a pro-fibrotic mediator. x160 23 Vanderbilt University Study Late PBI-4050 treatment increased kidney autophagy in db/db eNOS-/- mice Vehicle PBI-4050 Up‐regulation of autophagy is very important in the self‐repair process LC3A staining, a marker of autophagy. x160 24 Vanderbilt University Study Plasma insulin levels (ng/ml) A 7 A: In untreated mice, plasma insulin levels decrease gradually. * P < 0.05 vs. 8 wk; †P < 0.05 vs. 16 wk. 6 5 B: Early treatment with PBI-4050 (8 to 20 wks) prevents the decline of plasma insulin concentration. * P < 0.05 vs. vehicle. 4 3 * 2 1 0 8 † 16 C: Late treatment with PBI-4050 (16 to 24 wks) not only prevents the further loss of pancreas function, but restores pancreas function to that seen at 8 wk of age. ** P < 0.01 vs. vehicle; † P < 0.05 vs. baseline at 16 wk of age. 24 Age (week) C 7 Vehicle PBI-4050 * 6 5 4 3 2 1 8 week 20 week Plasma insulin levels (ng/ml) Plasma insulin levels (ng/ml) B 6 Vehicle PBI-4050 **† 5 4 3 2 † 1 0 16 week Insulin 24 week 25 Vanderbilt University Study 26 Vanderbilt University Study 27 PBI‐4547 Oral treatment with PBI-4547, a novel first-in-class anti-diabetic and anti-fibrotic compound, improves blood glucose level and kidney function in the diabetic db/db mouse model Lyne Gagnon, Kathy Hince, Liette Gervais, François Sarra-Bournet, Mikaël Tremblay, Marie-Pier Cloutier, Shaun Abbott, Jean-Simon Duceppe, Boulos Zacharie, Pierre Laurin and Brigitte Grouix PROMETIC BIOSCIENCES INC., LAVAL, QUÉBEC PBI-4547 reduces blood glucose level Photomicrographs expansion (X100) tissue showing mesangium F) 0.4 db/db 30 20 10 NX C57BL/6 NX db/db Day 0 B) NX db/db + PBI-4547 (10 mg/kg) Day 42 db/db + PBI-4547 (50 mg/kg) Histological Score 10 5 Day 0 Day 42 Day 42 D) p = 0.006 0 NX C57BL/6 NX db/db p = 0.008 NX db/db + NX db/db + PBI-4547 PBI-4547 (10 mg/kg) (50 mg/kg) Glucose/Insulin Ratio p = 0.09 5 Day 105 35 20 10 NX db/db NX db/db + NX db/db + PBI-4547 PBI-4547 (10 mg/kg) (50 mg/kg) PBI-4547 reduces mesangium lesions 1.0 0.5 p=0.0001 p=0.0001 p=0.0001 NX C57BL/6 NX db/db NX db/db + NX db/db + PBI-4547 PBI-4547 (10 mg/kg) (50 mg/kg) Day 105 25 15 p=0.068 0.1 0.0 NX db/db + PBI-4547 (50 mg/kg) PBI-4547 reduces insulin resistance (Day 42 and Day 105) 30 p=0.035 function 1.5 15 NX db/db + PBI-4547 (10 mg/kg) kidney 0.2 G) db/db + PBI-4547 (10 mg/kg) 20 C) p=0.016 Day 105 25 NX db/db increases 0.3 NX C57BL/6 PBI-4547 maintains or normalizes insulin level NX C57BL/6 PBI-4547 (GFR) 0.0 NX db/db + PBI-4547 (50 mg/kg) 30 25 20 15 10 p = 0.0002 p = 0.0003 p = 0.0003 5 0 NX C57BL/6 NX db/db PBI-4547 reduces blood triglyceride level 300 NX db/db + NX db/db + PBI-4547 PBI-4547 (10 mg/kg) (50 mg/kg) Triglycerides (mg/dl) Glucose (ng/ml) kidney 40 0 Glucose/Insulin Ratio of C57BL/6 50 0 Total nephrectomy of the right kidney was performed on day 0 and animals were treated with vehicle or PBI-4547 (10 and 50 mg/kg, oral once a day) from day 1 through 104. Kidney function (GFR) and kidney mesangium lesions were examined (PAS staining). Statistics: Student’s t-test E) 60 Insulin (ng/ml) STUDY DESIGN RESULTS A) GFR (ml/min/gBW) RATIONALE Worldwide, 171 million people have diabetes, and a number of complications are associated with poorly controlled hyperglycemia. Diabetic nephropathy is one of the most common complications of diabetes. Research points towards a multifactorial etiology and complex interplay of several pathogenic pathways that can contribute to the declining kidney function in diabetes. Obese and diabetic db/db mice exhibit a consistent mesangial matrix expansion. The aim of this study was to investigate the effect of PBI-4547 on blood glucose and insulin levels, and kidney function in uninephrectomized (NX) diabetic (db/db) mice. 200 p = 0.0024 100 0 p = 0.0002 NX C57BL/6 NX db/db NX db/db + NX db/db + PBI-4547 PBI-4547 (10 mg/kg) (50 mg/kg) 28 CONCLUSIONS PBI-4547: Reduces blood glucose level Maintains or normalizes insulin level Reduces insulin resistance (glucose-insulin ratio) Reduces blood triglyceride level Increases kidney function (GFR) Reduces mesangium lesions PBI-4547 offers the potential as a novel therapy for regulation of glucose metabolism and reduction of diabetic nephropathy. PBI‐4050 Clinical Program PBI-4050: Clinical Program H2 2014 Phase Ib Multiple doses DKD patients Safety & PK (Canada) 2015 Phase Ib / II DKD patients Multi center Study Placebo controlled – double blind (Canada & USA) Phase Ib / II Idiopathic Pulmonary Fibrosis (IPF) patients Multi center Study Open Label (Canada & UK) Phase Ib / II Orphan condition (TBA) Multi Center study Open label (Canada & UK & USA) Objectives of the program: Primary end points: • Safety & tolerability in patients • Effects on biomarkers for fibrosis in blood & urine • Effects on diabetes (when applicable) • Tissue analysis / biopsies (when applicable) Information on dosing Set the stage for phase II/III 29 Milestones to year‐end • To disclose an additional Orphan indication for PBI-4050 • To file the IGIV IND with the FDA • To disclose 2 additional PPPS™ derived Orphan Rx • To close partnering deals providing : • Financial contribution • Access to market • Additional manufacturing capacity • Revenue range for H2 2014 ($15 M - $20 M) • Subject to revenue recognition on licensing fees • Revenue significantly higher in Q4 30 2015 Outlook Development and Regulatory Milestones In 2015, the Company expect to • have 4 plasma‐derived Biopharmaceuticals in phase III • file a BLA for plasminogen • generate PBI‐4050 proof of concept data in humans (via multiple phase Ib/II) • advance 2 new small molecules to be ready to enter clinical program in Q1 2016 • Secure multiple Orphan Drug Designations Partnering Multiple partnerships with drugs in clinical stage to provide: • complementary expertise and financial contribution • Access to market Revenue Growth Increasing supply of Bioseparation affinity resins Sales of plasma‐derived proteins Expect strong H1 2015 31 Q&A 32
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